toasty7718

In addition to gaining weight, you'll also get cancer!

dude actually gave pretty decent health advice

"Dr." Eric Berg is a con-artist who sells more problems than solutions, I'm glad YouTube is finally pulling the plug on his channel. there's a reason why he never accepts any of the debates that he is invited to, especially on medical twitter. I'm not sure how I feel about YouTube censoring every anti-science video though. YouTube hasn't exactly been known to be the best company ever with good values and morals. I can easily see some abuse to happen with that.

@Sidra khanFrom what you're saying, it seems like you're looking to gain 5 kilograms of body weight in muscle mass, is that right? That should be your ideal goal when it comes to gaining weight - to prioritize gain in muscle mass. But unless you're pharmaceutically enhanced, that is going to be near impossible to accomplish without also gaining a little bit of fat, so expect that too. Here are the 6 ways to gain weight in a healthy way according go Dr. Spencer Nadolsky (I'll elaborate on each of them below) 1. Maintain a Hypercaloric state 2. Take your time 3. Palatable, more caloric foods 4. Adequate protein (no need to overdo it) 5. Resistance training 6. Light cardio for overall health 1. When it comes to losing weight, your goal should ideally be to burn more calories than you consume (in addition to healthy dietary patterns and better lifestyle habits like exercise) So the inverse is also true for gaining weight. You should prioritize eating more calories than you burn. But do keep in mind the subtle nuances found with this approach - example: you wouldn't want to gain weight by eating a bunch of Reese's cups 2. The only real way you can get super fast gains when it comes to weight gain with muscle is if you're pharmaceutically enhanced with steroids and / or growth hormones like IGF-1, and I'd assume you're not looking to go down that route As Dr. Nadolsky so elegantly puts it, take the "low and slow approach, a pound every other week" 3. If your overall goal is to gain weight, then you're not going to want eat a bunch of fruit and vegetable first in your meal because they fill you up and it's been demonstrated that those foods actually help people get leaner. Eat foods that are calorically dense and can be more easily overeaten. If it helps, here's a few charts demonstrating variability of different concentrations of calories in different types of foods. Here's a few examples of some healthy calorically-dense foods: - whole-grain pastas or legume-pastas (high in protein) - nut butters ( cashew, almond, pistachio, peanut, whichever you prefer really) - extra virgin olive oil, seed oils - avocados - greek yogurt (if you're not ethically objected to it) - dates, figs, raisins Essentially - you can add these foods to the diet that you normally eat as snacks and end up a caloric surplus Here's a few ideas for high-calorie smoothies: - 1 1/2 cups whole milk (or plant milks if you're ethically objected to it) - 2 small apples, washed and sliced - 1/3 cup rolled oats - 2 tbsp. almond butter - 2 tbsp. hemp seeds - 2 tbsp. chia seeds - 1 date - Cinnamon to taste - 2 handfuls ice cubes Most of these are variations on the same simple formula: milk (sourced from animals or plants, whichever you prefer), fruit (berries, bananas, apples, dates, figs, prunes, etc.), healthy sources of monounsaturated and/or polyunsaturated fats (nuts, seeds, nut butters, seed butters, maybe not oils because it tastes awful ) 4. You shouldn't need to consume over a gram of protein per pound of body weight (~2.2 grams per kilogram), ideally, you should strive for 1.6 grams of protein per kilogram of bodyweight. Here is a systematic review, meta-analysis, and meta-regression that pooled together 74 RCTs after a strict eligibility criteria was taken into effect to determine if increasing protein intake contributes to gaining muscle mass in healthy subjects. In short, the authors found that 1.6 grams of protein per kilogram of bodyweight should be ideal for maximizing muscle growth. Nunes, et. al. (2022) Systematic review and meta-analysis of protein intake to support muscle mass and function in healthy adults, Journal of Cachexia, Sarcopenia and Muscle, 13, 795–810, [https://doi.org/10.1002/jcsm.12922](https://doi.org/10.1002/jcsm.12922) "Alternatively, the evidence in this meta-analysis supports the hypothesis that additional protein ingestion (1.6 g of protein/kg/day or higher) leads to small increments in lean body mass in studies enrolling young subjects in RE training" There's only so much protein that can go towards building muscle, and once you cross that threshold you're losing out on the opportunity to be eating calorically-dense foods and foods that you enjoy if you're eating foods that are high in protein Here's a link to the PDF of a study that requires a paywall to get to: https://d1wqtxts1xzle7.cloudfront.net/74309445/ed5708ea38fe3115086b65fab63881765f7c-libre.pdf?1636324776=&response-content-disposition=inline%3B+filename%3DEffects_of_high_protein_diets_on_fat_fre.pdf&Expires=1694964869&Signature=P4Wn0ugJtD6mMyF8m60hCwGX5-jB9pF5l4Ee1SDvd-eUwwJ14Uc7gKRDXmYXNJ2tcSy-wDCgmD8L4bF2h4n3Dz5QNb-hQlPuoWcWz9hKlV8EHCktuNJmsbZgA6a5cEYmPJlGAZMidnTfir8qwlAJTyef-DMDy~1IAWsNUyiLBy6bQhsuW1Ehed38v6C1Y3AZQds4qHw9MEGvUfueO1Yd0-sNfTv7hQme37P1dpmEpK32e31K7vC4lFe5V4IcyBS6R8iG-QM56YBWPwaxqaQNG1Re~CPtEhi3t3Kbs7CXlJCOMrH~cscRNW9FkIb2T-1wmqDq9oSBhDpSAfMPqmSjdA__&Key-Pair-Id=APKAJLOHF5GGSLRBV4ZA "A randomized controlled trial of 39 adults assigned the subjects diets providing protein at 0.8 (recommended dietary allowance; RDA), 1.6 (2x RDA), and 2.4 (3x RDA) [...] In summary, we determined that consuming dietary protein at levels exceeding the RDA (1.6 grams / kilogram of body weight) may protect fat-free mass during short-term weight loss." Now, what about exercise? When it comes to weight-gain and virtually all aspects of health and longevity, exercise is just as important as nutrition. Peter Attia once said that nutrition is an asymmetric input; meaning, if you get it wrong, you're going to suffer the consequences. If you get it right, then you're going to have neutral benefits. If you want to see gains, then consider adopting a symmetric input like exercise. If you get it wrong, you'll suffer the consequences. If you get it right, you'll reap the benefits. Some people can lift weights but not see any benefit because their nutrition doesn't permit for it to happen. What lifting weights comes down to really is sending your body a signal to the damaged muscle and giving it the energy and nutrients it needs to repair. 5. Resistance training. 3 - 4 days a week should suffice. Look up resistance training videos on YouTube. Also - look up overload hypertrophy plan, there's many different plans out there for you to choose from, pick one that resonates with you your goal should be to get close to collapse / failure, not reach the point of collapse / failure. Then - after a few weeks or months, adding more volume to your exercise in the form of more weights, more reps, and more sets, and also reaching a point where your nutrition aids in your recovery. Here's a paper touting the numerous benefits that are associated with resistance training https://www.bewegenismedicijn.nl/files/downloads/kraemer_et_al._2002_-_resistance_training_for_health_and_performance.pdf "Its potential benefits on health and performance are numerous; it has been shown to reduce body fat, increase basal metabolic rate, decrease blood pressure and the cardiovascular demands to exercise, improve blood lipid profiles, glucose tolerance, and insulin sensitivity, increase muscle and connective tissue cross-sectional area, improve functional capacity, and relieve low back pain. Many improvements in physical function and athletic performance are associated with the increases in muscle strength, power, endurance, and hypertrophy observed during resistance training. The key element to effective resistance training is supervision by a qualified professional and the proper prescription of the program variables. Proper program design, ie, that which uses progressive overload, variation, and specificity, is essential to maximize the benefits associated with resistance training." Kraemer, W.J., Ratamess, N.A. & French, D.N. Resistance training for health and performance. Curr Sports Med Rep_, 165–171 (2002). https://doi.org/10.1007/s11932-002-0017-7 If you're new to exercise, then consider working with a personal trainer. It's not uncommon for those who start an exercise regimen to do too much too fast and fall of the horse very quickly. Your goal shouldn't be walk into the gym 20lbs underweight and want to walk out with a normal / healthy body-weight. That's Disneyland thinking. Your goal should be to apply yourself and push yourself out of your comfort zone on the regular to reap the benefits over a period of many weeks. It's not uncommon for females to be averse to lifting weights out of fear of getting too buff from them. This is something that is just not going to happen unless you're pharmaceutically enhanced. Muscles take a long time to grow in mass, and this is especially true for females because their metabolism and hormones differ from males. If anything, what you'll find is that you'll end up more toned and you'll fill out areas like your legs, abdomen, buttocks, and belly. Your arms will also get some shape and tone to them 6. You may have heard in the fitness sphere that "cardio will ruin your gains!" While this is mostly true if you're doing high-intensity cardio and you're not allocating enough time to rest and recovery, including low-intensity cardio as a part of your exercise regimen will actually yield many health benefits and contribute to your long-term health and longevity in addition to weight gain. This can take the form of aerobic exercise, for example. Here's some new research that's come out out in regards to musculoskeletal muscle hypertrophy (muscle growth) and aerobic exercise https://paulogentil.com/pdf/Skeletal Muscle Hypertrophy with Concurrent Exercise Training - Contrary Evidence for an Interference Effect.pdf "Based on the literature, we conclude that aerobic exercise training may facilitate resistance-training mediated hypertrophy if (1) exercise bouts are separated by 6–24 h, (2) concurrent exercise is performed using strategies that minimize overall exercise volume (i.e., utilizing high-intensity intervals, 2–3 days of aerobic exercise, B2 days of leg lifting), and (3) the mode of aerobic exercise favors cycling as opposed to running" You mentioned how you eat almost double than other girls. So from which I can assume that you're someone with a high metabolism. Metabolism refers to the rate at which your body's cells convert the calories from the food you consume into energy for various bodily functions. A high metabolism means your body works really fast to turn the food you eat into energy. It's like a super-fast engine that burns calories quickly, so you might find it harder to gain weight and may feel hungry more often. Measure your calories out over a day to get an idea of what you consume on the regular. My personal preference is an app called cronometer.com. In addition to tracking your calories, you can also use it to track all of your macronutrients and micronutrients All of this is under the assumption that you're healthy and there's no underlying medical issues (like thyroid problems) that can be causing you to lose weight and keep it off.

& sorry if I got a bit heated at times, I'm just passionate about evidence-based nutrition and find it appalling when people give health advice that has been demonstrated time and time again to result in detrimental health outcomes.

I mean it shows that it's possible. I'll grant it's possible that you're right; that's trivially true. What's the evidence that the claim is actually true? The body of the cake is that it doesn't actually demonstrate your claim, it just shows that it's theoretically possible. yeah, take care man, wish you the best. just don't be surprised when you start to develop CVD in your mid to late 30s

I see you've provided me with over 60 sources cited by authors of a paper entitled "Omega-6 vegetable oils as a driver of coronary heart disease: the oxidized linoleic acid hypothesis" This is a screen-snip from a paper by James J DiNicolantonio and James H O'Keefe. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6196963/ For starters, let's just examine the competing interests of the authors: "Competing interests: JD is the author of The Salt Fix and Superfuel and operates the website thesaltfix.com. JHO has an ownership interest in CardioTabs, a nutraceutical company" @Leo Gura so I suppose supplement is the easy way to make $$$, especially if you have mechanistic outcome data to back up your claims interesting ... I appreciate the evidence that you've given me from these two authors to support your proposition, but on first glance what I notice is an over abundance of mechanistic speculation. Why need mechanistic speculation when we have meta-analyses of prospective cohort studies showing that those with higher intakes or blood levels of linoleic acid have lower all-cause mortality, CVD incidence and mortality, stroke, and cancer mortality? https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7326588/ Let's examine some of the sources these unbiased authors cite, shall we Source (2) states: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4334131/ "Our findings suggest that adipose tissue LA has increased substantially in the United States over the last half century, and, to our knowledge, for the first time demonstrate that this increase is highly correlated with increased dietary LA intake over the same period ... Because LA is in involved in numerous physiologic and pathophysiologic processes, these changes have potentially significant implications for public health. These findings call for further research into the consequences, positive or negative, of such a major shift in the adipose tissue concentration of a single bioactive FA occurring over a relatively short period of time in the United States." Even the authors of that paper conclude that based purely on the increase of linoleic acid in adipose tissue requires further research to see if it has positive or negative health effects. Given the meta-analysis and epidemiologic studies that I've provided, all this paper does is prove my point even further They say with source (4) Linoleic acid serum concentrations (as opposed to per cent of fatty acids) are higher in patients with CAD https://pubmed.ncbi.nlm.nih.gov/8472362/ An interesting finding for sure, but how do we link it as being causal? What we need is an RCT that shows that increasing linoleic acid serum concentrations increased CAD compared to a control group, not looking at CAD and seeing that they have higher concentrations of it, you know? That's much better at determining causality. For source (3) they state linoleic acid in adipose tissue and platelets positively associates with CAD, whereas EPA and DHA in platelets are inversely correlated with CAD Another interesting finding. Again - correlation does not equate to causation. Also - this is a small sample size of 226 patients. Preferably, we want to have a large group of people to see if the effects are repeatable. Let's examine more robust studies - more specifically, meta-analyses preferably Just a side note: when it comes to correlation not equating to causation, an example I like to use is the fact that countries that smoke more live longer, or the fact that those who own lighters are more likely to have lung cancer, or the fact that some foods raise blood pressure so therefore they're bad. You know what else raises blood pressure? Exercise! Having sex! So we can't rule out something raising blood pressure short-term as being bad. https://www.sciencedirect.com/science/article/pii/S000291652200778X This is a systematic review and meta-analysis of prospective cohort studies to examine associations between LA intake and mortality (including, but not limited to CVD) It pooled together 38 studies with 44 prospective cohorts and included 811,069 participants (a far-cry from the 226 you mentioned earlier) To summarize, the authors finish the article by saying "In prospective cohort studies, higher LA intake, assessed by dietary surveys or biomarkers, was associated with a modestly lower risk of mortality from all causes, CVD, and cancer. These data support the potential long-term benefits of PUFA intake in lowering the risk of CVD and premature death." https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6582360/ This study was written by a whopping 59 PhD holding authors (I counted it, by the way) This is a harmonized, de nova, individual-level analyses in a global consortium of 30 prospective observational studies from 13 countries that looked at the circulating and adipose tissue LA biomarkers with total CVD and subtypes. Heterogeneity was explored by age, sex, race, diabetes, stain use, aspirin use, omega-3 levels, among others. In the prospective cohort studies ranging from 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659, and higher levels of LA were significantly associated with lower risks of total CVD and its subtypes They conclude by saying higher in vivo circulating and tissue levels of LA were associated with lower risk of major cardiovascular events. So - let's leave the reader with a choice. A study pool of hundreds of patients undergoing coronary angiography without heterogeneity taken into account vs. two meta-analyses of close to a million participants with sex, age, weight, habits, omega-3 intake, etc., taken into account and still finding that higher intake of PUFA contributes to lower risk of CVD. Your evidence is weak, suffice to say Source (5) doesn't contribute to your proposition either because it shows benefit of going on a weight loss high carb low fat diet, and one group high in MUFAs with beneficial effects of weight loss to lower risk factors of CVD https://pubmed.ncbi.nlm.nih.gov/9538963/ "MUFA-enriched hypocaloric diets potentiate the beneficial effects of weight loss to ameliorate cardiovascular risk factors in obese patients with type 2 diabetes." https://pubmed.ncbi.nlm.nih.gov/14739118/ From what I've seen, none of the studies they cited about oxidized LDL even make the slightest hint that oxidized LDL is caused by increased intake of PUFA, like seed oils. Also - measuring oxidized LDL is something that no cardiologist does because it's a meaningless metric. None of the studies they mentioned were adjusted against ApoB either because if it did, it would have no meaning. This paper touches on that and says that oxLDL should be compared with ApoB Viita, H., Närvänen, O., & Ylä-Herttuala, S. (1999). Different apolipoprotein B breakdown patterns in models of oxidized low density lipoprotein.. Life sciences, 65 8, 783-93 . https://doi.org/10.1016/S0024-3205(99)00305-7. "We suggest that in order to improve interpretation and comparison of results, data obtained with various models of oxidized LDL should be compared to the simplest and most reproducible models of 3 h and 18 h copper-oxidized LDL (apoB breakdown) and MDA-LDL (apoB aggregation) since different models of oxidized LDL have significant differences in apoB breakdown and aggregation patterns which may affect immunological and biological properties of oxidized LDL." To name some more of the studies they cited and the inconsistencies I see Sources (6), (53), (54), and (56) and models done on rodents, so I don't see any relevancy there in terms of human health-outcome data. Source 57 is funded by the National Cattleman's Beef Association, so it's best taken with a grain of salt. https://www.metabolismjournal.com/article/S0026-0495(00)97008-2/pdf I'm absolutely certain that more are sponsored by that, but... I don't feel like going through and picking out weak pieces of evidence. One of the sources concludes https://academic.oup.com/ajcn/article-abstract/75/2/221/4689295 "Increased ALA intakes decrease the estimated IHD risk to an extent similar to that found with increased LA intakes. Group nutritional education can effectively increase fish intake." This doesn't support their proposition either. RCTs like the LA Veterans study where they measured levels of linoleic acid in adipose tissue and the intervention group saw levels increase on the vegetable oil diet and a statistically significant reduction in heart disease. There's many more sources, but I don't really see a point in dismantling them all given the fact that a) the authors have a conflicting bias for their own supplement companies b) the first of the studies I mentioned were weak evidence c) the narrative just doesn't suddenly flip one day with nutrition science and foods are bad all of a sudden, you have to look at the totality of the evidence, and the totality of the evidence has leaned towards replacing SFA intake with PUFA intake to decrease risk of CVD d) correlation does not equate to causation e) the oxidized LDL hypothesis has no real bearing given the fact that the studies never compare it to ApoB (because if they did, it would expose it as a meaningless metric), and therefore no cardiologists use it f) there is much more robust evidence than mechanistic outcome data speculation g) the better evidence is in the form of a systematic review and meta-analysis of prospective cohort studies and / or RCTs with very large sample sizes (tens or hundreds of thousands of participants) of people with heterogeneity taken into account, written by authors with nuance and (preferably) without bias h) "USDA: moderate saturated fat AHA: moderate sat fat Canada: moderate sat fat UK: moderate sat fat Spain: moderate sat fat Australia: moderate sat fat China: moderate sat fat South Africa:moderate sat fat WHO:moderate sat fat" g) I'm getting tired of this TL,DR: the paper you took a screen snip of was written by two authors with conflicting biases for their own supplement companies and they rely mostly on mechanistic outcome data and speculation for their claims (and some of the sources even contradict their proposition). Why focus on that singular paper there is much more robust evidence in the form of a systematic reviews, meta-analysis, and prospective cohort studies which have hundreds of thousands of participants each? They examine the link between CVD with the intake of omega-6 and find that higher intake of linoleic acid decreases risk of CVD. At this point I really think you should concede on your proposition, but I find that unlikely to happen. I've debunked your pseduoscientific claims more than once and at this point I'm done with this debate. It takes me hours to compile the evidence (which don't get me wrong, I enjoy doing. It gives me an opportunity and reason to read into nutrition, which is something I'm interested in) I'll state again: misinformation kills people. What you're doing is a disservice to this whole forum.

That's interesting. what evidence do you have for your proposition about seed oils and heart disease?

jason I'm going to ask you again, What evidence for you have for this proposition?

I see, The seamless logic of ecological associations between the use of surgical interventions, like coronary artery bypass grafting, does explain at an epidemiological level the risk for CVD mortality going down, so we can't rule PUFA intake exclusively because there's an abundance of confounding factors. That's a logical fallacy on my part So for that reason, the intake of PUFAs and lowering of CVD mortality at a population wide scale isn't robust enough. I should specify that in terms of large scale RCTs, we don't really have large scale outcome trials on the effects of PUFA intake and CVD risk. Given the bulk of the evidence that has been accumulated over the past century, health experts have ruled that performing such an RCT to be unethical because it would mean upping the intake of SFA. The best evidence we currently have in terms of RCTs are trials that were completed decades ago. When it comes down to the observational evidence, what we find is that higher intake of PUFAs and MUFAs reduces CVD risk. This is a prospective cohort study done analyzing the intake of saturated fats, unsaturated fats, and carbs with CVD risk. It has a total of 127,536 participants and their diets were assessed by food frequency questionnaire every four years. It followed them for up to 30 years, and they found that higher intake of PUFAs and unrefined carbohydrates was associated with lower risk of CVD https://www.sciencedirect.com/science/article/pii/S0735109715046914 "During 24 to 30 years of follow-up, we documented 7,667 incident cases of CHD. Higher intakes of [PUFAs] and carbohydrates from whole grains were significantly associated with a lower risk of CHD [...] Our findings indicate that unsaturated fats, especially PUFAs, and/or high-quality carbohydrates can be used to replace saturated fats to reduce CHD risk." That's just observational evidence, is it not? How accurate even are FFQs? In truth, not very accurate. There are a multitude of pitfalls that come with self-reporting, so for that very reason, researches have resorted to measuring biomarkers (more on that later) Increasing your intake of saturated fat past a certain threshold increases your circulating levels of LDL cholesterol and ApoB. This is a study from the World Health Organization analyzing the effect of modifying of of SFA intake with MUFAs, PUFAs, and carbs, and here are the results they found: https://apps.who.int/iris/bitstream/handle/10665/246104/9789241565349-eng.pdf There was a 0.058 mmol/L change in LDL cholesterol per 1% of energy replaced when you replace calories from PUFAs with calories from SFAs, as compared with 0.019 mmol/L and 0.012 mmol/L with replacement with carbs and MUFAs, respectively. But do keep in mind that LDL cholesterol is a surrogate marker for atherogenic lipoproteins, and a much better metric would be apolipoprotein B (ApoB). The atherogenic lipoprotein molecules all have one molecule tag of ApoB. This includes: LDL, VLDL, Lp(a), chylomicron remnant particles, and IDL. And as such, what this table shows is that replacement of PUFAs with SFA marks a 10.3 mg/dL increase of ApoB particles in the blood. And as I've already noted before, ApoB increases risk for CVD and shortens life-span: https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext](https://www.thelancet.com/journals/lanhl/article/PIIS2666-7568(21)00086-6/fulltext "In conclusion, our evaluation of apoB using outcomes in first-degree relatives identified that higher apoB is detrimental to lifespan and increases the risk of coronary heart disease and type 2 diabetes. Lifestyle and pharmacological approaches to lowering ApoB should have widespread beneficial effects, including preventing common diseases and prolonging life." But when it comes to self reporting, it is well known that for large groups of people it reasonably helpful. Not so much for small groups of people in an RCT. Therein lies the reason why researchers have started using biomarkers instead of FFQs. This group of researches sought to evaluate how circulating levels of omega 6 fatty acids relate to the incidence of CVD, and it pooled together thirty studies from across the world. and their results are as follows: https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.118.038908 "In 30 prospective studies with medians of follow-up ranging 2.5 to 31.9 years, 15,198 incident cardiovascular events occurred among 68,659 participants. Higher levels of [Omega-6] were significantly associated with lower risks of total CVD, cardiovascular mortality, and ischemic stroke" So basically to summarize this, the links between increased PUFA consumption, CVD mortality, and the use of surgical interventions to deal with CVD are hypothesis generating pieces of evidence in of themselves, and much more robust evidence is needed to raise certainty in the domain of omega 6 rich seed oils and CVD risk. The preponderance of the evidence suggests that replacing SFA intake with PUFAs lowers your ApoB and decreases your risk of heart disease.

Increased linoleic acid consumptions marks the most significant change in CVD mortality over the last 100 years https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5268076/

Yea, too much of anything can be problematic

You still haven't given me any evidence for this proposition

I'm sorry, I don't understand. Can you provide a proposition to this statement?

Maybe do what Peter Santenello does & document what it's really like around the world and have one of the locals show you around for a 40+ minute video? His channel motto is something like "showing you the world the media doesn't show" or something like that.